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Query: UMLS:C0001511 (Adhesion)
 5,955 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Fibrin adhesives have been advocated as a protective sealant in high-risk colonic anastomoses to prevent leakage. To assess the effect of fibrin glue sealing on the healing ischemic anastomosis, we compared the healing of sutured colonic anastomoses in the rat, with and without fibrin adhesive (Groups IA and IB), and ischemic anastomoses with and without fibrin adhesive (Groups IIA and IIB). On days two, four, and seven, 10 animals in each group were sacrificed. Adhesion formation was scored, and the in situ bursting pressure was measured. The collagen concentration and degradation were estimated by measuring hydroxyproline. Adhesion formation was more prominent in Groups IB, IIA, and IIB on day four only; abscesses were noted in the ischemic group in four rats. Anastomotic bursting pressure was significantly lower in sealed (IB) and ischemic anastomoses (IIA) than in normal anastomoses (IA) on day four. Sealing of ischemic anastomoses did not change bursting pressures on days two, four, and seven. The relative decrease of collagen in the sealed anastomoses is significantly higher on day four only. It is concluded that sealing of normal colonic anastomoses in the rat has a negative effect on wound healing. Ischemia at the anastomotic site results in weaker anastomotic strength on day four postoperatively. Also in ischemic anastomoses, fibrin sealant does not improve wound healing during the first seven days. Adhesion formation on ischemic intestinal anastomoses was not prevented by fibrin sealing.
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PMID:Healing of ischemic colonic anastomosis: fibrin sealant does not improve wound healing. 151 51

Autologous fibrin gel (FG) has recently been reported efficacious in hepatic injury; the effects of fibrin compounds on intra-abdominal adhesion formation is controversial. This study evaluated intra-abdominal adhesion formation in a rabbit devascularization model. Seventeen New Zealand rabbits were anesthetized and laparotomy was done. The uterine horns were abraded to punctate bleeding followed by bilateral uterine devascularization. Treatment consisted of 10 cc saline control (c) or FG applied to the uterine horns. Peritoneal lavage was done at 15 minutes for red blood cell (RBC) analysis. Autopsy was performed at 1 week. Adhesions were graded from grade 0 (no adhesions) to grade III (dense adhesions). Adhesion grading revealed no difference in average adhesion grade between FG and C with small bowel (1.0 +/- 1.3 vs 0.5 +/- 1.0); bladder (2.1 +/- 1.1 vs 2.4 +/- 1.2); or uterus (1.2 +/- vs 2.0 +/- 1.2). Adhesion grade was significantly less in FG compared to C for the colon and the abdominal incision (0.4 +/- 0.5 vs 1.7 +/- 1.1 and 1.2 +/- 1.1 vs 3.0 +/- 1.2; P less than 0.05 by t-test). There were no differences in lavage RBC count between FG and C (13.1 x 106 +/- 4.1 x 10(6) vs 8.7 x 106 +/- 3.2 x 10(6)). Fibrin gel significantly decreased incisional and colonic adhesions and reduced other abdominal adhesion formation by a nonhemostatic dependent mechanism.
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PMID:Fibrin gel limits intra-abdominal adhesion formation. 152 26

Adhesion and spreading of cultured human umbilical vein endothelial cells on fibrin surfaces of varying structure were characterized to understand better the interactions occurring between endothelium and fibrin at sites of vascular injury. Fibrin prepared with reptilase, which cleaves only fibrinopeptide A from fibrinogen, and fibrin prepared with thrombin, which cleaves both fibrinopeptide A and fibrinopeptide B, equally supported endothelial cell adhesion. In contrast, only fibrin made with thrombin mediated endothelial cell spreading, as assessed by fluorescence microscopy of cells stained with rhodamine phalloidin to identify actin stress fibers or by scanning electron microscopy. Fibrin prepared with reptilase failed to support cell spreading. To further investigate the role of the amino terminus of the fibrin beta chain after fibrinopeptide B cleavage in promoting cell spreading, protease III from Crotalus atrox venom was used to specifically cleave the amino-terminal 42 residues of the fibrinogen B beta chain. After clotting with thrombin, this fibrin derivative lacking B beta 1-42 failed to support significant cell spreading. Spreading on fibrin was unaffected by depletion of Weibel-Palade bodies from endothelial cells, indicating that the spreading was independent of stimulated von Willebrand factor release. We conclude that endothelial cell spreading on fibrin requires fibrinopeptide B cleavage and involves residues 15-42 of the fibrin beta chain.
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PMID:Endothelial cell spreading on fibrin requires fibrinopeptide B cleavage and amino acid residues 15-42 of the beta chain. 154 76

To study platelet activation as a phenomenon that may precede development of angiopathy in diabetes mellitus, we compared platelet adhesion and thrombus formation in a flow system with blood from insulin-dependent (type I) diabetic subjects with and without macroangiopathy and age- and sex-matched control subjects. Adhesion and thrombus formation on matrix of cultured human endothelial cells (ECM) and adhesion on matrix of human fibroblasts (FBM) were studied after exposure to flowing blood at shear rates of 300 and 1300 s-1 and exposure times of 1, 3, 5, and 10 min (and 20 min in adhesion experiments). Blood was anticoagulated with trisodium citrate (1:10 vol/vol, 110 mM) or low-molecular-weight heparin ([LMWH] 20 U/ml). Endothelial cell cultures were either unstimulated or stimulated with 4 beta-phorbol 12-myristate 13-acetate (PMA) 16 h before isolating their matrix. Platelet adhesion on ECM and FBM in citrated and LMWH-anticoagulated blood was identical in diabetic patients and control subjects, with comparable increases of adhesion with increasing perfusion times. Platelet aggregate formation on ECM of PMA-stimulated cells with LMWH-anticoagulated blood was similar in diabetic patients, whether macroangiopathy was present, compared with control subjects. Fibrin deposition and fibrinopeptide A generation during perfusion were comparable in diabetic and control subjects. Platelet thromboxane B2 formation after stimulation with arachidonic acid was increased in diabetic patients without macroangiopathy compared with age- and sex-matched control subjects. In the perfusion system, the patterns of platelet adhesion and aggregate formation on extracellular matrix in flowing blood of diabetic patients (with or without macroangiopathy), and healthy age- and sex-matched control subjects followed a similar pattern.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Platelet adhesion and aggregate formation in type I diabetes under flow conditions. 193 2

Fibrin adhesives have been advocated as a protective seal in colonic anastomosis to prevent leakage. In order to assess the effect of fibrin glue sealing we compared the healing of sutured colonic anastomosis in the rat (group 1) with the addition of human-derived fibrin sealant (group 2). As a control for a possible reaction to foreign protein, in group 3 the sutured anastomosis was sealed with specially prepared rat fibrin adhesive. On days 2, 4 and 7, ten animals in each group were killed. Adhesion formation was scored and the in situ bursting pressure was measured. The collagen concentration and degradation were estimated by measuring hydroxyproline. Adhesion formation was significantly increased in groups 2 and 3 compared with the control group. On days 2 and 7 the bursting pressure was not different between the groups. On day 4 the bursting pressure in groups 2 and 3 was significantly lower than in group 1 (P less than 0.001). These findings correspond with the results of collagen measurements. On day 4 the concentration of hydroxyproline was significantly reduced in groups 2 and 3. Histological examination showed infiltration of neutrophilic granulocytes into the sealant on days 2 and 4; on day 7 the sealant had vanished. From these results it is concluded that fibrin sealing of the colonic anastomosis in the rat does not improve healing, as demonstrated by bursting pressure and hydroxyproline concentration. On the contrary, it seems to have a negative influence.
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PMID:Effect of fibrin sealant on the healing colonic anastomosis in the rat. 187 28

The objective of the research was to determine the effect of the type, dose, and volume of anti-fibrinolytic agents (tranexamic acid, aprotinin) added to fibrin formulations, on adhesion development. Adhesions were induced in 228 male rats by creating apposing parietal and visceral peritoneal defects. Animals were randomized to receive no treatment or a fibrin formulation containing aprotinin or tranexamic acid. Seven days later the incidence of adhesions, and the force and energy required to detach them, were determined. Adhesions developed in 13/13 rats in the control and aprotinin groups. Treatment with fibrin (100 mg/ml tranexamic acid) resulted in adhesions in 4/14 rats (as strips, p < or = 0.0005), 4/10 rats (as spray, p < or = 0.0036), and 12/15 rats (by drip). The reduction of adhesions was dependent on the concentration of tranexamic acid with strip and spray application. Using commercial formulations, tranexamic-acid-containing fibrin (10/15, p = 0.042), but not aprotinin-containing fibrin (13/15), reduced the incidence of side-wall adhesions from 15/15 in controls. Fibrin containing either tranexamic or aprotinin reduced the incidence and severity of adhesions. This effect was greater when tranexamic acid was used and was dependent on the mode of administration, the volume, and to a degree, the concentration of tranexamic acid.
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PMID:The effect of tranexamic acid in fibrin sealant on adhesion formation in the rat. 1473 72

Fibrin sealants can be used to support tissue regeneration or as vehicles for delivery of cells in tissue engineering. Differences in the composition of fibrin sealants, however, could determine the success of such applications. The results presented in this article show clear differences between Fibrin sealant A (FS A) clots and Fibrin sealant B (FS B) clots with respect to their compatibility with primary human cells involved in soft tissue repair. FS A clots, which are characterized by a physiological coarse fibrin structure, promoted attachment, spreading, and proliferation of keratinocytes, fibroblasts, and endothelial cells. In contrast, FS B clots displaying a fine to medium clot structure failed to support spreading of all three cell types. Adhesion of keratinocytes was decreased on FS B clots compared to FS A clots after 3 h incubation, whereas number of attached fibroblasts and endothelial cells was initially comparable between the two fibrin sealants. However, all three cell types proliferated on FS A clots but no sustained proliferation was detected on FS B clots. We further demonstrate that the observed differences between FS A and B clots are partly based upon 1 M sodium chloride extractable constituents, like thrombin, and partly on nonextractable constituents or the fibrin structure. In conclusion, our in vitro results demonstrate that FS A clots serve as a provisional matrix that encourages adhesion and growth of keratinocytes, fibroblasts, and endothelial cells. Therefore, FS A seems to be well suited for applications in tissue engineering.
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PMID:Cell compatibility of fibrin sealants: in vitro study with cells involved in soft tissue repair. 2062 47

Fibrin glue-soaked gelatin sponge (FGGS) has been used for tissue sealing in neurosurgical practice, but too rapid clotting of fibrin glue occasionally prevents good fixation of FGGS. Dilution of thrombin may provide adequate manipulation time between mixing fibrinogen and thrombin on gelatin sponge and application into the tissue defects. The present study characterized the effect of thrombin dilution on the adhesion strength of FGGS and retrospectively assessed the clinical usage of the dilution for filling dead space or sealing arachnoid defect in 255 cases who underwent transsphenoidal surgery for the last 66 months. FGGS was prepared using three different concentrations of thrombin: 250 (standard), 50 (1:5 dilution), and 25 (1:10 dilution) units/ml, and incubated for three different periods (5, 20, and 60 seconds). FGGSs were applied over two adjacently positioned porcine skins placed on two metallic plates. The adhesion strength was evaluated by measuring maximum tensile strength during pulling out the sliding plate at a constant rate of displacement. The maximum adhesion strength was greater for FGGS with 1:10 diluted thrombin solution than for FGGS prepared with higher concentrations (p < 0.05). Adhesion strength did not decay for 20 seconds after the mixture. Only four of 255 cases (1.6%) required second reconstruction of sella floor due to the cerebrospinal fluid leakage. FGGS prepared with diluted thrombin solution can provide adequate adhesion strength for clinical use.
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PMID:Effect of thrombin concentration on the adhesion strength and clinical application of fibrin glue-soaked sponge. 2335 64